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At least 973 records · Page 54Linked to original sources
PubMed2004

Nondiabetic ketoacidosis caused by severe hyperthyroidism.

Severe hyperthyroidism is not included in the traditional differential diagnosis of ketoacidosis. However, thyroid hormone has well-documented lipolytic effects on adipocytes and may also promote hepatic beta-oxidation. We present a case in which a woman with severe hyperthyroidism developed otherwise unexplained ketoacidosis during the acute phase of her illness. We propose that thyrotoxicosis was a significant contributor to ketoacidosis in this patient and that severe hyperthyroidism should be added to the differential diagnosis of ketoacidosis.

Acidosis↗
PubMed1978

Acute abdominal pain precipitated by phenformin-associated lactic acidosis.

Phenformin-associated lactic acidosis is an important though unusual cause of acute abdominal pain. Its clinical picture suggests other catastrophic abdominal entities. A representative case is presented. Aids to arriving at this diagnosis are presented and the specific therapy is outlined. The pathophysiology of this condition is discussed.

Abdomen↗
PubMed2006

The impact of new comorbidities on nutritional status in continuous ambulatory peritoneal dialysis patients.

OBJECTIVE: To study the prevalence and risk factors for malnutrition in a peritoneal dialysis (PD) center with an active PD program. METHODS: We assessed the nutritional status in 205 continuous ambulatory peritoneal dialysis (CAPD) patients, including stable and unstable patients, by subjective global assessment (SGA), dietary diaries and biochemistry index. Serum C-reactive protein (CRP) levels were examined as inflammatory marker. Fluid status including extracellular water (ECW), intracellular water, and total body water (TBW) was evaluated by multiple-frequency bioelectrical impedance analysis and brachial blood pressure was measured. New comorbidities included systemic infection, congestive heart failure and trauma that occurred within 1 month or less. Cardiovascular disease (CVD) was recorded too. Dialysis adequacy and residual renal function were calculated by a standard technique. RESULTS: Based on SGA, 15.6% of our CAPD patients were malnourished. The malnourished patients had advanced age, higher CRP and ECW/TBW levels than normally nourished patients (age: 68.78 +/- 11.92 vs. 59.26 +/- 13.46 years, p = 0.001; CRP: 11.98 +/- 20.22 vs. 5.56 +/- 8.30 mg/l, p = 0.004; ECW/TBW: 0.55 +/- 0.16 vs. 0.52 +/- 0.04, p = 0.049). Patients with malnutrition were more prone to have CVD (53.13 vs. 31.79%, p = 0.004) and new comorbidities (65.62 vs. 4.62%, p = 0.023). Multivariate analysis showed new comorbidities, mostly systemic infection, which were associated with nutritional status (p < 0.001). Both ECW/TBW and new comorbidities were associated with serum CRP, CVD and malnutrition (p < 0.001-0.05). In contrast, some traditional factors which were recognized as contributing to malnutrition such as residual renal function, dialysis adequacy, metabolic acidosis, total protein loss, diabetes and Charlson indexes were not different between normally nourished and malnourished patients in the present study. CONCLUSIONS: Our results suggest that only 15.6% of patients were malnourished in our PD program. Old age, inflammation, CVD, fluid overload and new comorbidities were all associated with malnutrition, with new comorbidities, mostly systemic infections, being the most significant risk factor. However, many traditional factors such as residual renal function, dialysis adequacy and diabetes were not.

Age Factors↗
PubMed1977

Renal tubular abnormalities in a patient with the phenotypic appearance of C-trisomy mosaicism.

In 1971, SINHA et al. described a patient with isochromosomes arising from a C-group autosome. This patient had the phenotypic appearance of C-trisomy mosaicism. Six years later she presented with complaints of polydipsia and polyuria and was documented to have nephrogenic diabetes insipidus and renal tubular acidosis. The abnormal cell line of the patient had disappeared at the time of this observation.

Acidosis, Renal Tubular↗
PubMed2004

Proximal tubular dysfunction in primary Sjögren's syndrome: a clinicopathological study of 2 cases.

Tubulointerstitial nephritis is the most common renal complication in primary Sjögren's syndrome (SS). It is usually associated with symptoms of distal tubular dysfunction, type I (distal) renal tubular acidosis (RTA) and nephrogenic diabetes insipidus. Proximal tubular abnormalities are considered to be less frequent, and Fanconi's syndrome has been only exceptionally reported in patients with SS. We describe 2 patients with primary SS, characterized by xerostomia, dry eyes, extensive lymphocytic infiltrate on salivary gland biopsy, positive tests for anti-SSA/SSB antibodies and/or antinuclear antibodies, who presented in renal failure with proteinuria, microscopic hematuria and type I RTA. Further studies revealed proximal tubular dysfunction, including renal glucosuria, generalized aminoaciduria, phosphaturia, uricosuria, together with proximal (type II) RTA in 1 case. Neither of these patients had Bence Jones proteinuria or monoclonal gammopathy. Kidney biopsy showed focal proximal tubulitis, associated with proximal tubular cell atrophy and dedifferentiation, and diffuse interstitial nephritis with fibrosis. No significant glomerular or peritubular deposits of immunoglobulin light or heavy chain were observed. These findings demonstrate that diffuse, distal and proximal, tubular dysfunction may occur in patients with SS and interstitial nephritis. Lymphocytic infiltration of proximal tubular cells is probably involved in the pathogenesis of Fanconi's syndrome in SS. However, the mechanisms involved in the alteration of sodium-dependent apical transports remain to be elucidated.

Adult↗
PubMed1977

Phenformin-associated lactic acidosis: pathogenesis and treatment.

Since phenformin's introduction into clinical medicine, a total of 552 cases of lactic acidosis have been reported in patients taking this hypoglycemic agent. In 306 cases, sufficient documentation was available to establish the diagnosis with reasonable certainty (blood lactate, 6 meq/litre or greater, and blood pH, 7.33 or less). The mortality rate among insulin-treated patients (15%) was considerably less than the mortality rate in the group as a whole (42%). Taken together with results from animal studies, these data suggest that insulin is the treatment of choice for phenformin-associated lactic acidosis. Sodium bicarbonate should be administered to patients with severe acidosis, but should be withheld from patients with mild acidosis. Overly aggressive administration of sodium bicarbonate can be deleterious and should be avoided. Although dialysis has been suggested by some authors for the treatment of phenformin-associated lactic acidosis, the mortality rate among dialyzed patients (48%) was roughly the same as for the group as a whole (42%).

Acidosis↗
PubMed1980

Lactate homeostasis and lactic acidosis.

The roles of changes in cellular redox, interorgan lactate flux and balance, and quantitative aspects of lactate metabolism in the pathogenesis of lactic acidosis are discussed. Altered metabolism of pyruvate is central to the development of lactic acidosis and hyperlactatemia. Lactic acidosis occurs as a result of a relative or absolute imbalance in lactate production and utilization. Lactate utilization for oxidative purposes and for the resynthesis of glucose is essential for the maintenance of acid-base balance. Because of its role in lactate homeostasis the liver may play a central role in acid-base balance. Impairment of hepatic utilization of lactate may produce lactic acidosis.

Acidosis↗